Reversal of the Locked-In State by Intra-Arterial Thrombolysis
April 1, 1998 3 minutes read
Reversal of the Locked-In State by Intra-Arterial Thrombolysis
ABSTRACT & COMMENTARY
Source: Wijdicks EFM, et al. Intra-arterial thrombolysis in acute basilar artery thromboembolism: The initial Mayo Clinic experience. Mayo Clin Proc 1997;72:1005-1013.
The great appeal of thrombolytic therapy to both physicians and lay persons derives from its potential to reverse even severe neurological deficits. Thrombolytic therapy by dissolving thrombi in occluded vessels restores perfusion to ischemic but still viable brain tissue before infarction occurs. Nowhere has brain salvage been so dramatically demonstrated as in this report.
Wijdicks and colleagues describe their recent experience with the intra-arterial delivery of the thrombolytic drug urokinase to treat acute basilar artery occlusions in nine patients. Before treatment, all had major neurological deficits due to acute brainstem ischemia. Two of them, a 76-year-old man with an atherothrombotic basilar artery occlusion and a 27-year-old woman with a patent foramen ovale and an embolic basilar artery occlusion, had quadriplegia and paralysis of the facial and oral muscles with preserved consciousness-the locked-in syndrome.
Basilar artery recanalization was successful in seven of nine patients treated within 13 hours (median, 4 hours) after the onset of symptoms. The two patients in whom basilar artery recanalization did not occur died in coma. Two patients had no neurological improvement despite recanalization and remained severely disabled and dependent. The remaining five patients had good outcomes with either complete recovery (4 patients) or recovery of independence with a slight hemiparesis.
Complications of thrombolytic therapy included a cerebellar hemorrhage without clinical worsening in one patient and retroperitoneal hematomas in two patients.
COMMENTARY
The results of this small series, judged in terms of successful basilar artery recanalization (78%) and of clinical recovery (56%), support the view of Caplan and others that intra-arterial delivery of thrombolytic agents is preferable to intravenous administration in cases of carotid or basilar artery occlusion (Neuro Alert 1998;16: 35). The full recovery of two locked-in patients is noteworthy in itself but is especially so because the time from onset of symptoms to thrombolysis was so long: 11 hours in the elderly man and 13 hours in the young woman. The delay in the first was due to the fact that arteriography and thrombolytic therapy was not considered until the patient's deficits had progressed over several hours to quadriplegia. In the second case, the onset of the locked-in state was sudden but occurred at another hospital, and delay resulted from the need to transfer the patient elsewhere for diagnostic and therapeutic intervention.
These results can be compared to those of the larger series of Brandt et al who treated 51 patients with acute basilar occlusions (Stroke 1996;27:875-881). They found that patients treated with intra-arterial thrombolytic drugs more than eight hours after onset still had recanalization and obtained a good clinical outcome. Therefore, these studies mean that, although timing is important in instituting thrombolytic therapy, in patients with acute basilar artery occlusions, it is still possible to take the time to obtain brain imaging studies and cerebral angiography before instituting intra-arterial thrombolysis without giving up a good clinical result. -jjc
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